DSM-5 and Eating Disorders

DSM-5 and Eating Disorders

The advent of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition(DSM-5) is a great opportunity to mark where we are as specialists in understanding eating disorders. It is also a moment to contemplate and applaud most of the changes in the diagnostic nomenclature, as they should aid significantly in the clinician’s ability to “officially” diagnose and label, provide earlier clinical intervention, and (hopefully) be reimbursed for these increasingly prevalent and debilitating diseases.

There are important changes for many psychiatric diagnoses in DSM-5, including several comorbid diagnoses frequently associated with eating disorders. However, my goal in this limited discourse is to highlight the logical and clinically relevant evolution of the DSM section on eating disorders. But I would be remiss in the area of clinical utility if I did not take a moment to briefly discuss the rationale for thinking diagnostically, as well as the benefit of considering comorbidity. In attempting to understand and treat eating disorders, there are many benefits for our patients in doing so.

My frame of reference is that of a treating and supervising psychiatrist who has specialized in treating eating disorders with more than 20 years in both inpatient and outpatient settings. I have been fortunate enough to work with hundreds of patients across the severity spectrum—from those ambulatory to those prostrate with life-threatening medical complications; from the neophyte beginning to experiment with eating disordered behaviors to those, unfortunately, chronically ill.

Overall considerations for DSM-5

Elimination of the Multi-Axial System

The MAS has been eliminated in DSM-5. The non-axial listing was previously an option in DSM-IV, but now this will become the norm. The clinician simply lists diagnoses, starting with the primary diagnosis (main reason for treatment), followed by other relevant psychiatric and medical conditions (formerly DSM-IV Axis I, II, and III diagnoses). (In the interest of brevity, the reader is referred to the Introduction section of the Manual as to the rationale for this change.)

Diagnoses are not designated by axis, and there is no listing of formerly Axis IV (Psychosocial Problems) and V (Assessment of Functioning) characteristics.

Elimination of “Not Otherwise Specified”

In DSM-5, the diagnostic category “Not Otherwise Specified” (NOS) has been replaced by two designations: (1) “Other Specified” and (2) “Unspecified.” This change applies to all psychiatric diagnoses, including eating disorders. If one is unable to specify one of the established listed diagnoses, such as Anorexia Nervosa, for example, one may diagnose by preceding the general category with (1) or (2) above. In this case, a clinician might choose “Other Specified Feeding and Eating Disorder” or “Unspecified FED” (see example below).

Eating Disorders in DSM-5: General Features

From ED to FED

The most obvious change from DSM-IV to DSM-5 is the change in the name of the specialty itself from “Eating Disorders” to “Feeding and Eating Disorders.” In the past year, I have been to several presentations on DSM-5 but have not heard highlighted the obvious pun in the acronym FED. In indulging my compulsion to do so here, I implore all eating disorder specialists to revel in our uniqueness; we are likely the only medical or psychiatric specialty for which the secret to a successful therapeutic outcome is revealed in the simple abbreviation of its name!

From Three to Eight

Equally of note, the number of eating disorder diagnoses in DSM-5 has increased from three to eight. These include six specific diagnoses: (1) Pica, (2) Rumination Disorder (RD), (3) Avoidant/Restrictive Food Intake Disorder (ARFID), (4) Anorexia Nervosa (AN), (5) Bulimia Nervosa (BN), and (6) Binge Eating Disorder (BED). They also include two “umbrella” diagnoses: (7) Other Specified Feeding or Eating Disorder (OSFED) and (8) Unspecified Feeding or Eating Disorder (UFED). To review the complete criteria for these diagnoses, the reader is again referred to the DSM-5 text (as well as elsewhere in this catalog).

DIAGNOSTIC CHANGES AND CLINICAL RELEVANCE

The diagnoses Pica and Rumination Disorder were both transferred from the previous DSM-IV section of “Disorders Usually First Diagnosed in Infancy, Early Childhood, or Adolescence” (now eliminated). Also in the same section, the diagnosis “Feeding Disorder in Infancy or Early Childhood”, (FDIEC), has been expanded and transferred to the new general category of Feeding and Eating Disorders. In this transformation, the name changes to “Avoidant/Restrictive Food Intake Disorder” or by its acronym, ARFID. Unlike FDIEC, ARFID can be diagnosed past age 6.

Given that the essential feature of Pica involves the repeated eating of non-nutritive, non-food substances, and given the mutually exclusive classification scheme for DSM-5 eating disorders, it is the only Feeding and Eating Disorder which can be diagnosed simultaneously with another eating disorder.

Rumination behavior, which involves the regurgitation of food which is then either re-chewed, re-swallowed or spit out, may exist as part of active AN or BN or as a sole diagnosis, Rumination Disorder. It may remain as a residual problem after apparent recovery from another eating disorder and may go undetected unless it is suspected and inquired about, since patients may not be forthcoming about its existence. This may give the practitioner a flawed complacency that the patient is in full recovery. A recent patient of mine illustrates this point:

M.D., a 44 year old mother of three in remission from restricting and over-exercising AN had a stable healthy weight for three years, even though she continued to express body dissatisfaction. During one meeting in response to more pointed questioning, she revealed that for years she had been and was still engaging in regurgitating and spitting out her food. She had previously not revealed this information, citing profound guilt and shame.

ARFID, a diagnostic category, encompasses a broad set of eating disordered behaviors e.g., from feeding problems of infancy to restrictive eating in a young adult afraid of choking. The reason for including these behaviors in the same diagnostic category may seem obscure initially. But the common feature here is that in these cases the eating refusal (and eventual negative medical consequences), do not stem from physical limitations; it is psychological but not based on distorted body image or weight concerns.

Many patients with the type of ARFID related to a desire to avoid aversive consequences (e.g., choking or vomiting) would have been diagnosed as EDNOS using DSM-IV. This often resulted in such problems as patients erroneously being confused as atypical anorexics or having trouble with third party reimbursement. This problem should now be rectified as these patients are placed into a specific diagnostic category with descriptive criteria.

Anorexia Nervosa

a) 85% is not a Marker. While there are no major conceptual developments, there are significant welcome changes to the criteria for Anorexia Nervosa. One clinically relevant difference is the use of the phrase “significantly low body weight” in Criterion A to replace the phrase “body weight less than 85% of that expected”. Significantly low weight is defined as less than minimally normal (adults) and less than minimally expected (children and adolescents) in the context of age, sex development and physical health. This new phrasing allows the clinician’s judgment to enter the picture as opposed to adhering to a rigid percentage of ideal or expected body weight as a criterion.

The irony here is that the abbreviation “e.g.,” (for the Latin term exempli gratia), meaning for example, was often confused by even the most erudite among us with “i.e.”, (short for Latin id est) which means that is. Therefore “for example 85%” converted in many minds to, “that is 85%” and this became gospel for diagnosing AN not only by clinicians and some patients who used it to deny their illness, but also insurance companies in denial of reimbursement.

So in DSM-5, the diagnosis of AN can be made above the 85% mark. In DSM IV, many cases meeting all criteria for AN but were 85 or higher percentage of IBW were diagnosed as Eating Disorder Not Otherwise specified (EDNOS). The perception of undue vagueness in utilizing the new criteria can be avoided by specifying severity according to a suggested scale as follows: Mild (BMI >or =17), Moderate (16-16.99), Severe (15-15.99) and Extreme (< 15). DSM-5 chose the starting point of BMI of 17 because of the World Health Organization’s standard. (The use of BMI for this scale will be controversial for some, as it does not account for differences in body type, bone structure, and muscle vs. fat differential. Further discussion is beyond the scope of this article).

b) Focus on Behavior. Criterion B also undergoes clinically relevant modification. To the relatively subjective designation of “intense fear of gaining weight or becoming fat” is added “persistent behavior that interferes with weight gain.” The emphasis here is not only on the patient’s mental attitude (which may be hidden by denial or even at times by a resistant patient’s desire to evade diagnosis and treatment) but also on behavior, which is more easily observed and measured.

c) Amenorrhea is absent. Perhaps the most obvious and clinically relevant development is the removal of amenorrhea from the diagnostic criteria for females. This eliminates a false “diagnostic imbalance” between males and females. It also allows official inclusion of the small percentage of females who manage to retain menstrual functioning despite extreme weight loss and malnutrition, and eliminates diagnostic concern over whether a client on hormonal replacement to induce menses is truly has amenorrhea.

With previous criteria in DSM-IV some patients who had not lost their menses but otherwise had AN behaviors and weight loss, could argue that they did not have the diagnosis. Many clinicians have thought that amenorrhea was best considered a medical complication of weight loss in anorexic females, rather than being a diagnostic criterion, e.g. similar to bradycardia or lanugo.

All of these changes help to create a diagnostic environment where a patient’s specific and sometimes objectively quantifiable behavior, as well as illness mindset, becomes the diagnostic focus. Utilizing DSM-5 clinicians should be able to utilize diagnostic guidelines and their clinical judgment to diagnose AN and intervene earlier in the course of illness, potentially reducing morbidity and chronicity.

Bulimia Nervosa

a) Fewer Episodes Required. The essential change in the diagnostic criteria for BN is the decrease in frequency of binge episodes and compensatory behaviors required to make the diagnosis. In DSM-IV one needed two or more episodes per week of binge eating and compensatory behaviors over a 3-month period to qualify for the diagnosis. In DSM-5, only one episode per week is required over the same time frame. Similar to AN, a severity specifier for the compensatory behaviors allows the clinician a more precise qualification: Mild (an average of 1-3 episodes of inappropriate compensatory behaviors per week), Moderate (4-7), Severe (8-13) and Extreme (>or =14).

Again the trend here is towards earlier official diagnosis by decreasing the frequency of behaviors required. Qualitatively is there a significant difference in clinical urgency between one who purges once vs. twice a week? Given evidence that most destructive potentially addictive behaviors are more responsive to treatment earlier in their course, any action, which allows sooner recognition and intervention, is welcome.

Binge Eating Disorder

a) Into the Mainstream. Having been lifted from the Appendix section of DSM-IV, BED is now an official psychiatric diagnosis in DSM-5. The rationale for this move was that following extensive research the “clinical utility and validity” of this condition were documented.

In addition, in moving from a research diagnosis, to a clinical one, the frequency of binge episodes required is reduced from a minimum of 2 days of binge episodes per week for 6 months, to one episode weekly for 3 months. Similar to AN and BN a severity specifier scale is offered, with the frequency of binges for each level being the same as the compensatory behaviors for BN: Mild (1-3 binge-eating episodes per week), Moderate (4-7), Severe (8-13) and Extreme (>0r= 14).

Under DSM-IV BED sufferers were usually given the diagnosis of EDNOS. The theme of inclusion and the clinician’s ability to diagnose earlier after the onset of symptoms, continue with the DSM-5 addition of BED as an official Feeding and Eating Disorders Diagnosis.

Other Specified Feeding or Eating Disorder and Unspecified Feeding or Eating Disorder

a) EDNOS Splits Up. As mentioned above it has been replaced in DSM-5 with OSFED and UFED. One of these diagnoses should be used in cases where distressful and impairing symptoms of an eating disorder are present, but the full criteria for one of the other FED’s are not met. The difference between the two is that in OSFED the specific reason is stated, but in UFED it is not. In the latter case it may be that not enough information is available to decide what type of FED is present.

An OSFED example could be a patient who started out at a high body weight who then lost significantly via an anorexic restricting pattern who has body image distortion, fear of weight gain, but whose current weight is still normal. It might be listed as “Other Specified Feeding or Eating Disorder: Anorexia Nervosa Currently at Normal Weight”. A UFED example could be a normal weight patient who admits to binging and purging “once or twice” in the last 3 months (suspected of more), has undue concerns with body weight and shape, and uses no other compensatory behaviors. It would simply be listed as “Unspecified Feeding or Eating Disorder”.

SUMMARY OF CHANGES AND POSSIBLE SIGNIFICANCE

In scrutinizing the new developments in Feeding and Eating Disorders in DSM-5 one is impressed with two main trends, i.e., inclusivity and lowering of criteria for diagnosing some illnesses. Rumination Disorder, Avoidant/Restrictive Food Intake Disorder and Binge Eating Disorder have now been added as official diagnoses. Criteria have changed for AN and BN allowing diagnosis for less severe symptom use and earlier in the illness course. In AN, objective behavior that interferes with weight gain can replace the subjective and potentially reticent criterion of fear of weight gain. All these modifications should result in less use of the former EDNOS (now OSFED and UFED). Though clearly unintended, the use of EDNOS often had the erroneous effect of minimizing the seriousness of eating disorders. In some situations third party payers balked at reimbursing for the EDNOS diagnosis. The DSM-5 changes should promote earlier diagnosis and clinical intervention, could help potentially lower morbidity and chronicity, and ideally, improve reimbursement.

DIAGNOSIS AND COMORBIDITY: FOOD FOR THOUGHT

With DSM-5, mental health clinicians in general and eating disorders clinicians in particular, have at their disposal the most researched and deliberated diagnostic manual in Psychiatry’s history. Why do we need such a manual? By learning the diagnostic nomenclature, it helps clinicians speak a common language and communicate with each other about our patients. Thinking diagnostically about patients encourages us to generally organize our thinking about their illness, allows us to make some hopefully valid assumptions about associated features (including psychosocial aspects), which usually accompany a diagnosis. But perhaps most importantly, making a diagnostic formulation helps to inform treatment, increasingly so as evidenced based treatments become the norm.

Once diagnostic formulations are made, they should be regularly reviewed, by those who made them as well as clinicians who inherit a patient with a particular diagnosis. They should be assessed both for accuracy and agreement amongst clinicians as well as being up to date. Accurate diagnosing of FED utilizing DSM-5 criteria should not pose major challenges for the average clinician. Well-honed interviewing skills and an ability to match historical data to the criteria obtained from a thorough interview and appropriate physical assessment will usually produce accurate diagnoses.

Astute clinicians cannot think diagnostically about the main condition that brings the patient to treatment, without pondering deeply what other clinical features or syndromes might also be influencing the development, course and potential treatment of the primary problem. One must also consider comorbidity. Unlike DSM-IV, DSM-5 has a “Comorbidity” section for each of the FED diagnoses. Even though not extensively discussed, many of the other common psychiatric diagnoses associated with the particular eating disorder diagnosis are mentioned. E.g., “Bipolar, depressive and anxiety disorders commonly co-occur with anorexia nervosa. Many individuals with anorexia nervosa report the presence of either an anxiety disorder or symptoms prior to onset of their eating disorder…”

As a clinician beginning to specialize in eating disorders almost 25 years ago I was soon surprised by how many patients appeared to have mood and anxiety disorders in addition to severe eating disturbance and how these conditions frequently persisted after stabilization of the eating disorder. Working with children and adolescents, pre-morbid histories could often be obtained showing pre-existing anxiety and mood disturbances before any eating disordered behavior emerged. Furthermore there was likely to be family history of anxiety, mood or substance use disorders. Over the years my clinical experience has continued to witness this pattern, and some of the most successful and lasting interventions for the eating disorder, have not come until stabilization of the comorbid disorder. However I continue to see patients with eating disorders who have had previous treatment for whom there has been no mention or significant discussion of the comorbid diagnosis, even in a few instances where the latter condition was more exigent than the eating disorder.

Eating disorders are psychiatric disturbances where likely a confluence of dysfunctional brain mechanisms influenced by environmental factors result in abnormal feeding and eating behavior. This leads to physical changes and medical complications in those afflicted, as well as further mental changes. It is likely that comorbid psychiatric disorders strongly influence the dysfunctional brain mechanisms (for example leading to altered perceptions, greater impulsivity or compulsivity) thereby predisposing to eating disordered behavior. (It is also possible that comorbid disturbances are perhaps manifestations themselves of the same brain dysfunction.)

Whether comorbid conditions help to “drive” eating disordered cognitions and behavior or whether they arise as expressions of the same brain deregulation, it would seem that with greater comorbidity, eating disorders become more difficult to treat and have higher degree of chronicity. For example, a bulimic patient suffering from untreated Bipolar Disorder, which places her in a more highly “reactive” or deregulated state, will be more likely to binge and purge when confronted with triggers.

Comorbid factors influence not only manifestations of the eating disorder, but also response to treatment. An adolescent suffering from unrecognized or untreated PTSD, when feeling “trapped” might experience unmanageable fright and terror from any treatment intervention perceived as coercive whether in a hospital treatment program or family (home) based setting.

In co-occurring situations, the treatment of one disorder can exacerbate or complicate the treatment of the other. For example a bulimic patient who is failing CBT and DBT treatment and who refuses potentially effective medication for her mood disorder due to fear of weight gain side effects, risks continued decrease in impulse control and poor response to other modalities. This results in continued debilitation from both illnesses.

Comorbid conditions combined with an eating disorder result in poorer quality of life than an eating disorder alone. The panic level anxiety felt by a child with ARFID at mealtimes is also likely to have been experienced by him through other diagnosable anxiety spectrum disorders, such as separation anxiety, school phobia or OCD. Successful therapeutic attention to his anxiety disorder can result not only in resolution of the eating disturbance and subsequent medical complications, but also improved functioning in other areas of his life as well.

With co-occurring disorders an increased likelihood of chronicity exists for both conditions if either is not adequately managed. There is potential mutual exacerbation since the cognitions and behaviors from the comorbid disorder often intensify disordered eating and the latter, through the effect of nutritional derangement on brain chemistry, worsen the comorbid disorder.

There is lack of clarity sometimes as to whether certain comorbid traits reach the threshold of a diagnosable condition. There has been general debate in the field and often confusion in a particular case, whether a comorbid diagnosable condition precedes and/or is causative to an eating disorder or results from it. But just as it is important to consider cognitive and behavioral changes caused by malnutrition and starvation, it is incumbent to recognize those, which might precede and exacerbate FED. Comorbidities may be hidden because of focus on the more visible physical changes of the FED, and threat of medical consequences. But to always assume these changes result from FED presents a risk of incomplete treatment, continued morbidity, poor life quality and higher risk of FED relapse. Clinical experience and judgment are necessary, along with wise use of consultation.

The argument over whether or when to treat a patient who is malnourished, for an apparent mood or anxiety disorder which may be interfering with FED treatment is legitimate. The picture is tilted by the fact that when medications are being considered in an eating disordered patient, there is currently only one FDA-approved medication for any eating disorder: fluoxetine for bulimia. And yet despite potentially undesirable side effects, medications have been increasingly used over the last several years as part of the overall management of FED’s. As mentioned earlier I have witnessed cases where the results of ameliorating comorbid illnesses with medications have had dramatic positive benefit in recovery from an ED. Nevertheless I would hope that the current trend is due to a desire to target comorbidity and the recognition that treating co-occurring conditions can be a significant facilitator to successful overall treatment of FED, rather than a naively sought clinical coup de grace.

Finally, in this brief discussion on comorbidity I have been focusing mainly on psychiatric conditions that stand alone as diagnoses often requiring treatment or may coexist with other maladies such as FED. These diagnostic “connections” are recognized in DSM-5 and point to a common biogenetic substrate and psychosocial underpinnings in the final pathway to the development of serious psychiatric disturbances whether eating or other disorders. They also summon into action a variety of analytic and therapeutic skills whether present in an individual clinician, or spread across different professionals comprising a treatment “team”. However I want to make sure that despite the focus on comorbidities that are diagnosable entities with strong biological determinants, eating disorders according to my experience, clearly are not solely brain-based disorders. Despite recent trends by the profession to emphasize biogenetic factors in causation, FED are paramount examples of biopsychosocial illnesses. As often as I have seen the missing piece to the recovery puzzle in eating disorders be the elimination of another comorbid psychiatric disorder, I have also seen it be the resolution of a psychosocial “comorbidity”. Eating disorders are richly complex, multi-determined illnesses. It is this phenomenon that has stimulated, humbled and held me captive as a clinician for the last 22 years.